benserazide has been researched along with Friedreich Ataxia in 2 studies
Benserazide: An inhibitor of DOPA DECARBOXYLASE that does not enter the central nervous system. It is often given with LEVODOPA in the treatment of parkinsonism to prevent the conversion of levodopa to dopamine in the periphery, thereby increasing the amount that reaches the central nervous system and reducing the required dose. It has no antiparkinson actions when given alone.
benserazide : A carbohydrazide that results from the formal condensation of the carboxy group of DL-serine with the primary amino group of 4-(hydrazinylmethyl)benzene-1,2,3-triol. An aromatic-L-amino-acid decarboxylase inhibitor (DOPA decarboxylase inhibitor) that does not enter the central nervous system, it is used as its hydrochloride salt as an adjunct to levodopa in the treatment of parkinsonism. By preventing the conversion of levodopa to dopamine in the periphery, it causes an increase in the amount of levodopa reaching the central nervous system and so reduces the required dose. Benserazide has no antiparkinson actions when given alone.
Friedreich Ataxia: An autosomal recessive disease, usually of childhood onset, characterized pathologically by degeneration of the spinocerebellar tracts, posterior columns, and to a lesser extent the corticospinal tracts. Clinical manifestations include GAIT ATAXIA, pes cavus, speech impairment, lateral curvature of spine, rhythmic head tremor, kyphoscoliosis, congestive heart failure (secondary to a cardiomyopathy), and lower extremity weakness. Most forms of this condition are associated with a mutation in a gene on chromosome 9, at band q13, which codes for the mitochondrial protein frataxin. (From Adams et al., Principles of Neurology, 6th ed, p1081; N Engl J Med 1996 Oct 17;335(16):1169-75) The severity of Friedreich ataxia associated with expansion of GAA repeats in the first intron of the frataxin gene correlates with the number of trinucleotide repeats. (From Durr et al, N Engl J Med 1996 Oct 17;335(16):1169-75)
| Excerpt | Relevance | Reference |
|---|---|---|
| "A quantitative evaluation of cerebellar ataxia, with an ataxia score (total, static, kinetic) and the measurement of objective values relating to the major symptoms, was used in 21 patients with hereditary ataxias treated for 12 months with high doses (16 mg/kg/day) of d-l-5-HTP, l-5-HTP or the combination d-l-5-HTP (16 mg/kg/day)--benserazide (6 mg/kg/day)." | 7.67 | Regression of cerebellar syndrome with long-term administration of 5-HTP or the combination 5-HTP-benserazide. ( Trouillas, P, 1984) |
| "A quantitative evaluation of cerebellar ataxia, with an ataxia score (total, static, kinetic) and the measurement of objective values relating to the major symptoms, was used in 21 patients with hereditary ataxias treated for 12 months with high doses (16 mg/kg/day) of d-l-5-HTP, l-5-HTP or the combination d-l-5-HTP (16 mg/kg/day)--benserazide (6 mg/kg/day)." | 3.67 | Regression of cerebellar syndrome with long-term administration of 5-HTP or the combination 5-HTP-benserazide. ( Trouillas, P, 1984) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 2 (100.00) | 18.7374 |
| 1990's | 0 (0.00) | 18.2507 |
| 2000's | 0 (0.00) | 29.6817 |
| 2010's | 0 (0.00) | 24.3611 |
| 2020's | 0 (0.00) | 2.80 |
| Authors | Studies |
|---|---|
| Trouillas, P | 2 |
| Garde, A | 1 |
| Robert, JM | 1 |
| Adeleine, P | 1 |
2 other studies available for benserazide and Friedreich Ataxia
| Article | Year |
|---|---|
Regression of cerebellar syndrome with long-term administration of 5-HTP or the combination 5-HTP-benserazide.
Topics: 5-Hydroxytryptophan; Benserazide; Cerebellar Ataxia; Dopamine; Drug Therapy, Combination; Friedreich | 1984 |
[Regression of human cerebellar ataxia under long term administration of 5-hydroxytryptophan].
Topics: 5-Hydroxytryptophan; Adult; Benserazide; Cerebellar Ataxia; Female; Friedreich Ataxia; Humans; Male; | 1981 |